Shadows in the Light: Moonshine’s White Lightning and Vision Loss

Abstract

Methanol poisoning remains an important cause of severe metabolic and neurologic toxicity, most commonly resulting from ingestion of illicit or improperly distilled alcoholic beverages such as Moonshine. We report a case of acute methanol toxicity following Moonshine ingestion, presenting with central nervous system manifestations and visual symptoms. The patient experienced rapid clinical and visual improvement after timely treatment with fomepizole and emergent hemodialysis. In addition to standard therapy, corticosteroids were administered as an adjunctive treatment for visual involvement. This case highlights the importance of early recognition and prompt extracorporeal clearance in methanol poisoning and explores the potential role of corticosteroids as an adjunct in patients presenting with visual symptoms.

1. Introduction

Despite decades of published literature and established treatment guidelines, methanol poisoning continues to be a clinically significant cause of optic nerve injury and high-anion gap metabolic acidosis.1 Even though industrial exposures or widespread outbreaks of tainted alcohol account for the majority of reported cases, occasional consumption of illegally distilled beverages, like moonshine, still happens and can make diagnosis difficult, especially if co-ingested ethanol postpones the onset of symptoms.2 Formic acid, which is produced when methanol is broken down, damages the retina and optic nerve specifically, possibly resulting in irreversible vision loss.3 Although the mainstays of treatment are fomepizole and extracorporeal removal, the function of adjunctive corticosteroids in methanol-associated optic neuropathy is still unclear, and there is little clinical evidence to support their use.4 This case reports early biochemical correction and favorable visual recovery due to early detection of methanol toxicity after moonshine ingestion, prompt initiation of fomepizole, emergent hemodialysis, and adjunctive high-dose corticosteroids for visual involvement. This report adds to the small body of research investigating corticosteroids as a possible adjunct in methanol-induced optic neuropathy by emphasizing early multimodal intervention in a sporadic exposure. Conclusions about causality or steroid efficacy are still limited because this is a single-patient observation; nevertheless, the case emphasizes the significance of early clinical suspicion and multidisciplinary management to avoid irreversible neurologic sequelae.

2. Case description

This is a 27-year-old-man with history of poly-substance use disorder, ADHD and bipolar disorder, who presented with a one-day history of progressive malaise associated with a generalized headache, nausea, vomiting (non-bloody, non-bilious) and photophobia. He reported alcohol consumption in the form of moonshine mixed with juice with friends one day prior.

Upon arrival, the patient was afebrile, heart rate was 81 bpm, respiratory rate of 18 breaths/min with a blood pressure of 143/99 mmHg that later normalized to 121/89 mmHg and oxygen saturation of 99%. EKG showed sinus bradycardia with a ventricular rate of 51 bpm. His neurologic exam was non focal and had no relative afferent defect.

Labs were significant for an anion gap metabolic acidosis of 22, pH of 7.00 on Venous Blood Gas (VBG) with a pCO2 of 26 mmHg suggestive of metabolic acidemia. Albumin-corrected anion gap ratio of 0.5 suggestive of pure high anion gap metabolic acidosis. Lactic Acid was 3 mmol/L. There was no history suspicious of salicylate or ethylene glycol ingestion. Initial Measured Osmolarity was 345 mOsm/kg with an osmolar gap of 64 mOsm/kg.

The potassium was 4.8 mmol/L, creatinine was 1.12 mg/dL and Beta-Hydroxybutyrate was elevated at 0.54 mmol/L. Urinalysis showed mild ketonuria (15) and pH of 6.0. The ethanol level was undetectable. Urine drug screen was positive for cannabinoids, and a methanol level and ethylene glycol were sent for specialized testing given notoriety of moonshine.

Due to high concern for methanol intoxication in the setting of new-onset visual symptoms, anion gap metabolic acidosis, and mild acute kidney injury (AKI) without crystals in the urine, he was given a loading dose of fomepizole and started on a bicarbonate infusion prior to emergent hemodialysis. He was also was started on medical treatment with fomepizole maintenance, high dose folic acid regimen, thiamine and pyridoxine. His symptoms significantly improved. Repeat blood work showed hypokalemia, hypophosphatemia, mild alkalosis and a repeat osmolar gap that was narrowed to 15. Nephrology team opted to hold hemodialysis due to lack of confirmation of methanol levels and significant improvement of the acidosis. Given persistent light sensitivity despite aggressive treatment, pulse corticosteroids therapy was recommended by retina specialists. However, a lower dose regimen was started given uncertainty of benefit and history of underlying psychiatric illness. Due to persistent symptoms, the ICU team discussed with nephrology, and the patient received a second session of hemodialysis after which symptoms resolved completely. The repeat osmolar gap was less than 5. His corticosteroids course was reduced further given an episode of psychosis and agitation while in the ICU.

Three days later, by the time of discharge, the methanol level initially drawn was found to be elevated at a severely critical level (145 mg/dl; Toxic> 20 mg/dL) and, as expected, the ethylene glycol was undetectable (<10 mg/L).

3. Discussion

Methanol poisoning is a life-threatening cause of high anion gap metabolic acidosis and neurologic dysfunction, classically associated with visual impairment. Although toxic alcohol ingestion may be diagnostically challenging, the presence of metabolic acidosis with an elevated osmolal gap should raise early concern, even though either abnormality may be absent depending on timing of presentation.5 Compared with ethylene glycol intoxication, which commonly progresses to cardiopulmonary complications and acute kidney injury, methanol poisoning typically presents with visual and neurologic manifestations, as seen in our patient.1 Timing and early recognition of methanol toxicity is crucial, especially when signs of end-organ damage are present such as acidosis and retinal toxicity, perceived as visual symptoms.

The mechanism of retinal toxicity results from the metabolic conversion of methanol to formic acid, which causes selective damage to the optic nerve through mitochondrial dysfunction.6 Methanol is metabolized by alcohol dehydrogenase to formaldehyde, which is then oxidized to formic acid by formaldehyde dehydrogenase.6 The toxic metabolite formic acid inhibits cytochrome c oxidase in the mitochondrial oxidative phosphorylation pathway, leading to cellular energy failure.7 This mechanism results in selective damage to the papillomacular bundle, which is particularly vulnerable due to its high metabolic demands.8

Management of methanol toxicity includes close monitoring of cardio-respiratory status in the ICU and prompt medical management as described below. Even though rare, in a patient known to have ingested a large amount of methanol or ethylene glycol who presents within 60 min of the ingestion usually gastric aspiration via flexible nasogastric tubing is recommended. Otherwise, activated charcoal, gastric lavage, and syrup of ipecac have no routine role in the management of toxic alcohol exposures.5 Our patient was way outside the window.

Furthermore, mainstay treatment includes antidotes that work by competitive inhibition of alcohol dehydrogenase with intravenous fomepizole to prevent formation of the toxic metabolite, formic acid. If fomepizole is not available, intravenous ethanol also competes with other alcohols to reduce toxic metabolite formation.5

Equally effective, extracorporeal therapy in the form of hemodialysis rapidly and effectively removes toxic alcohols and is often initiated early in confirmed ethylene glycol or methanol poisoning, as well as in suspected cases associated with high anion gap metabolic acidosis or evidence of endorgan damage, such as visual impairment or kidney injury, as seen in our patient. Recommended indications for extracorporeal treatment including any of the following being attributed to methanol: coma, seizures, new vision deficits, metabolic acidosis with blood pH ≤ 7.15, persistent metabolic acidosis despite adequate supportive measures and antidotes, serum anion gap higher than 24 mmol/L; or, serum methanol concentration 1) greater than 700 mg/L (21.8 mmol/L) in the context of fomepizole therapy, 2) greater than 600 mg/L or 18.7 mmol/L in the context of ethanol treatment, 3) greater than 500 mg/L or 15.6 mmol/L in the absence of an alcohol dehydrogenase blocker9; in the absence of a methanol concentration, the osmolal/osmolar gap may be informative as was our case. Our patient met all indication for extracorporeal treatment given a severely toxic level of 145 mg/dL (ie, 1450 mg/L).

In a patient with a blood pH < 7.25 and a strong suspicion or confirmed ethylene glycol or methanol poisoning, treatment with sodium bicarbonate is strongly recommended. We begin treatment with 1 to 2 meq/kg of sodium bicarbonate via IV bolus followed by an infusion.2

The early stage of methanol-induced optic nerve injury is thought to parallel the pathophysiological features of optic neuritis.7,10 Based on this similarity, glucocorticoids have been used in the management of methanol-induced optic neuropathy due to their ability to suppress pro-inflammatory cytokine activity, enhance anti-inflammatory pathways, and provide neuroprotective and anti-demy-elinating effects.10 In reported cases, glucocorticoids are typically administered as high-dose intravenous methylprednisolone at 1 g daily for 3–4 consecutive days, followed by an oral prednisolone regimen of approximately 1 mg per kilogram of weight daily.4,7,11,12

The existing data on the use of steroids for prevention or treatment of methanol-induced optic neuropathy consist of uncontrolled interventional case series with wide variability in patients, treatment regimens, and outcomes.4,7,9,12,13 A primate model demonstrated lack of benefit from steroids, and human experience suggests that variable vision recovery after methanol poisoning occurs in the absence of steroid treatment, calling any dose-response effect of steroids into question. Some data suggest potential benefit when steroids are initiated early after methanol ingestion but routine use cannot be recommended based on current evidence. 10,11,14 In the case of our patient, visual symptoms were assessed subjectively given lack of in-house ophthalmology. It would have been definitely more interesting to see objective improvement in visual acuity with the use of steroids. Additionally, given concerns for an underlying psychiatric disorder and a brief episode of psychosis, we opted against pulse steroid therapy as recommended by the poison control and used a lower dose for a lower period of time, of unclear benefit, and the patient required a supplemental dose.

4. Conclusion

This case underscores the risks of methanol ingestion from homemade alcohol, resulting in severe systemic toxicity and associated visual complications. This case reinforces the importance of initiating treatment based on clinical suspicion and exposure history, even before confirmatory methanol levels are available, to prevent permanent visual loss and mortality.